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目的 研究酪氨酸蛋白磷酸酶 (PTP)抑制剂钒酸钠对缺氧海马突触体膜 (synapticplasmamembranes,SPM)磷酸酪氨酸蛋白 (p -tyr-pr)含量及神经元损伤的影响。方法 采用大鼠海马脑片体外缺氧模型 ,建立了p-tyr-pr测定的ELISA法 ,观察了PTP抑制剂钒酸钠对缺氧大鼠海马脑片突触体膜中p -tyr-pr含量及脑片孵育上清液中乳酸脱氢酶 (LDH)漏出量的影响。结果 缺氧引起SPM中p -tyr -pr含量下降 ;缺氧前 15min加入钒酸钠 ,则p -tyr-pr显著增加 ,同时LDH漏出量明显升高 ,且其漏出量增加与钒酸钠浓度呈剂量依赖关系。结论 蛋白酪氨酸磷酸化的增加可能起加重缺血性脑损伤的作用。
Objective To investigate the effect of sodium vanadate, a tyrosine protein phosphatase (PTP) inhibitor, on the content of p-tyr-p and neuronal damage in hypoxic hippocampal synaptosomal membrane (SPM). Methods The rat model of hippocampal slices in vitro hypoxia was established by the p-tyr-pr assay ELISA was observed PTP inhibitor sodium vanadate hippocampal slices of rat hippocampal synaptic membrane p-tyr-pr Content and brain lactate supernatant lactate dehydrogenase (LDH) leakage. Results The content of p -tyr -pr in SPM was decreased by hypoxia. When sodium vanadate was added 15 min before hypoxia, p -tyr-pr increased significantly and the leakage of LDH increased significantly. The leakage increased with the concentration of sodium vanadate In a dose-dependent manner. Conclusion The increase of protein tyrosine phosphorylation may play an important role in ischemic brain injury.